Long-term potentiation of transmitter release induced by repetitive presynaptic activities in bull-frog sympathetic ganglia.

Long-lasting potentiation of transmitter release induced by repetitive presynaptic activities in bull-frog sympathetic ganglia was studied by recording intracellularly fast excitatory post-synaptic potentials (fast e.p.s.p.s.). Following a brief period of post-tetanic potentiation or depression (less than 10 min), the amplitude of the fast e.p.s.p. was potentiated for a period between several tens of minutes and more than 2 h in response to tetanic stimulation of the preganglionic nerve in twenty-one out of twenty-eight cells. Quantal analysis revealed that this long-term potentiation of the fast e.p.s.p. (l.t.p.) was accompanied by an increase in quantal content m (in nine out of twenty-one cells), quantal size (four cells) or both (eight cells). The increased quantal content (presynaptic l.t.p.) declined exponentially (ten cells) or decayed gradually to a certain enhanced level which lasted several hours. In contrast, the increased quantal size grew with a relatively long latency (10-25 min) and remained relatively constant for at least 2 h. The magnitude of presynaptic l.t.p. increased with increased duration of the presynaptic tetanus (33 Hz) from 2 to 5 s. No l.t.p. was elicited by a 1-s tetanus, whereas the time course appears to be independent of the tetanus duration and the magnitude of l.t.p. There was a positive correlation between the magnitude of presynaptic l.t.p. and the pre-tetanic quantal content up to m = 3, but the former deviated from linear regression when the value of the latter exceeded 3. No l.t.p. occurred when quantal content was less than 0.5. A tetanus (33 Hz, 10 s) applied in Ca2+-free solution elicited no presynaptic l.t.p., while the same tetanus in normal Ringer solution produced a large presynaptic l.t.p. Presynaptic l.t.p. was enhanced in magnitude at low temperature (8-10 degrees C). These results demonstrate the existence of a use-dependent, long-term potentiation of transmitter release in bull-frog sympathetic ganglia. Several possible mechanisms are discussed in terms of Ca2+-buffering mechanisms of the presynaptic nerve terminals.